ReviewNeoplasia (New York, N.Y.)2026
Targeting tumor dormancy: the next frontier in gastrointestinal stromal tumor therapy.
Review in Neoplasia (New York, N.Y.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastrointestinal stromal tumors (GISTs), the most common mesenchymal neoplasms of the digestive tract, are primarily driven by mutations in KIT/PDGFRA. The remarkable success of tyrosine kinase inhibitors such as imatinib (IM) in treating GIST has established them as a paradigm of precision medicine in modern oncology. However, acquired resistance to IM remains a major cause of poor prognosis in GIST patients. Exploring novel mechanisms of IM resistance is critically important for improving outcomes. Tumor dormancy and cancer stem cell (CSC) models, observed across multiple malignancies, are closely linked to therapy resistance, tumor recurrence, and metastasis. Emerging evidence suggests that analogous non-genetic persistence states also exist in GIST, including dormant cells and KIT
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.